This study revealed the link between sleep duration and overweight or obesity in adolescents of Fuzhou, China. After adjusting socio-demographic status, lifestyle factors, and mental health, there was a negative correlation between sleep duration and overweight or obesity among male children.
The prevalence of overweight or obesity in our study was 19.2%, which was higher than the national average [2]. Moreover, our findings demonstrated the differences among gender, age and region, which were similar with the Report on Childhood Obesity in China [18]. The prevalence of obesity showed decline with the elevation of the ages, which may be possibly related to physical development and attention to their appearances. The prevalence of obesity in male children was significantly higher than that of female children. In addition, the prevalence of sleep deprivation in adolescents showed strike increase with age. About 92.4% of adolescents in high school suffered from sleep deprivation. Study pressure, especially pressure from the college entrance examination, may contribute to such a high prevalence.
Our study revealed that sleep duration was negatively related to obese risk, which was consistent with previous study showing that sleep deficiency seemed to parallel the increased prevalence of obesity[19]. Meanwhile, it could be an independent risk factor for obesity[7, 20, 21]. One study provided causal evidence on the relationship between sleep deprivation and weight gain in the population-level [22]. Moreover, Krietsch et al reported that there was a U-shaped correlation between those with insufficient sleep and obesity only in the female children [23]. These differences may be related to the physiology of adolescence between female and male.
To date, little is known about the relationship between sleep and obesity. Sleep duration involved in the regulation of cerebral function such as controlling the appetite, which could lead to over-eating in an obesogenic environment [24]. The homeostatic control of appetite was achieved by complex interactions among numerous neuroendocrine hormones [25]. Many pivotal hormones (e.g. insulin, leptin, cortisol and ghrelin) [26] may involve in the correlation between sleep and obesity. Even after adjusting the BMI, sleep duration was negatively correlated with circulating leptin [27]. Eptin pathway could explain the key mechanism via a modification effect [28]. Under some circumstances, the sleep deprivation could lead to disruption of insulin, leptin, cortisol and ghrelin expression [29, 30]. After a period of sleep loss, people could experience a 24% increase in hunger with largely whetting the appetite for high carbohydrate foods [29]. In our study, students with short sleep duration spent more time on night snack than those with adequate sleep, which may lead to weight gain. Fatigue caused by insufficient sleep may result in reduced physical activity, which then promoted the weight gain [31, 32]. In this study, adolescents with adequate sleep did more exercise of moderate-intensity than those with insufficient sleep.
Circadian Locomotor Output Cycles Kaput (CLOCK) genes involved in regulation of diurnal rhythm, and their effects on neuroendocrine systems might have an impact on obesity [33]. The variants of CLOCK gene was related to sleep duration [34], as with calorie intake [35], metabolic syndrome [36], and obesity [37]. Meanwhile, methylation of CLOCK gene was associated with carbohydrate intake, total energy intake, insulin resistance, and BMI [38]. REV-ERBα rs2071570 and rs2071427 were related to BMI and sleep duration in male children, confirming the association of the REV-ERBα gene with human obesity, mainly in males [39]. In line with our findings, this theory supported a negative correction between sleep duration and overweight/obesity only among male children [40].
A large and representative sample was included in the survey. Meanwhile, we analyzed a wide range of covariance to verify the relationships between sleep duration and overweight or obesity by adjusting potential confounding factors correlated with overweight or obesity. Nevertheless, there are some limitations in our study. First, causal inference will be limited in the cross-sectional design, although there are several theories supporting our findings. Second, the impact of prolonged sleep duration on overweight or obesity among adolescents was not explored in our study, as we laid emphasis on the risk of overweight or obesity induced by sleep deprivation in middle-school students.